front 1 A patient has pelvic pain and purulent-appearing discharge. Most
likely pathogen? | back 1 C. HSV-2 |
front 2 During active genital HSV, latency is established in: | back 2 A. Lumbosacral nerve ganglia |
front 3 Pregnant patient with primary active genital HSV at delivery. Best
management? | back 3 D. Cesarean section |
front 4 Molluscum contagiosum is caused by a: | back 4 B. Poxvirus |
front 5 MCV-2 is most commonly transmitted via: | back 5 A. Sexual contact |
front 6 Pearly dome-shaped papules with central dimple suggest: | back 6 C. Molluscum contagiosum |
front 7 Molluscum viral inclusions are located in the: | back 7 B. Cytoplasm |
front 8 Thick vulvovaginal erythema and swelling with “curd-like” discharge
is most associated with: | back 8 D. Candida |
front 9 The discharge classically described for Candida is: | back 9 A. Curd-like discharge |
front 10 Trichomonas vaginalis is best described as a: | back 10 C. Flagellated protozoan |
front 11 Post–spontaneous/induced abortion infections that can cause PID are
often: | back 11 B. Puerperal infections |
front 12 Puerperal infections spread upward via: | back 12 C. Lymphatic and venous channels |
front 13 Compared with gonococcal PID, puerperal infections tend to
inflame: | back 13 A. Deeper organ layers |
front 14 Smooth white vulvar plaques that enlarge/coalesce suggest: | back 14 B. Lichen sclerosus |
front 15 Advanced lichen sclerosus can lead to: | back 15 D. Constricted vaginal orifice |
front 16 Key histologic feature of lichen sclerosus is: | back 16 A. Epidermal thinning |
front 17 Squamous cell hyperplasia (lichen simplex chronicus) is driven
by: | back 17 B. Chronic scratching/rubbing |
front 18 Squamous cell hyperplasia is characterized by: | back 18 D. Epidermal thickening |
front 19 Both lichen sclerosus and squamous hyperplasia often show: | back 19 C. Hyperkeratosis |
front 20 Vulvar squamous papillomas are best described as: | back 20 B. Benign exophytic papilloma |
front 21 Most common histologic type of vulvar cancer is: | back 21 C. Squamous cell carcinoma |
front 22 Basaloid and warty vulvar carcinomas arise from: | back 22 D. Classic VIN |
front 23 Keratinizing vulvar SCC most often arises from: | back 23 D. Differentiated VIN |
front 24 Differentiated VIN is most associated with a history of: | back 24 B. Chronic lichen sclerosus |
front 25 A sharply circumscribed nodule on labia majora/interlabial fold
suggests: | back 25 C. Papillary hidradenoma |
front 26 Papillary hidradenoma histology shows: | back 26 D. Two-layer glandular lining |
front 27 Basaloid and warty vulvar carcinomas are: | back 27 B. HPV-related |
front 28 Basaloid and warty vulvar carcinomas typically occur: | back 28 A. At younger ages |
front 29 A vulvar carcinoma subtype is not HPV-related. Which is
it? | back 29 C. Keratinizing squamous carcinoma |
front 30 Keratinizing vulvar SCC occurs most often in: | back 30 A. Older women |
front 31 Keratinizing vulvar SCC is best described as: | back 31 D. More common than warty |
front 32 Pruritic red, crusted, maplike vulvar lesion suggests: | back 32 B. Extramammary Paget disease |
front 33 Extramammary Paget disease is usually on the: | back 33 A. Labia majora |
front 34 A lateral vaginal wall cyst from duct rests is: | back 34 B. Gartner duct cyst |
front 35 Gartner duct cysts are most often found on the: | back 35 D. Lateral vaginal walls |
front 36 Gartner duct cysts are typically: | back 36 A. Submucosal, fluid-filled cysts |
front 37 Virtually all primary vaginal cancers are: | back 37 C. Squamous cell carcinoma |
front 38 Primary vaginal SCC is strongly associated with: | back 38 D. High-risk HPV |
front 39 Vaginal SCC often arises from a premalignant: | back 39 B. VAIN |
front 40 The cervical site most susceptible to HPV is: | back 40 C. Immature metaplastic cells |
front 41 HPV primarily infects which epithelial cells? | back 41 A. Immature basal cells |
front 42 HPV cannot infect directly the: | back 42 B. Mature superficial squamous cells |
front 43 HPV infection of vagina/vulva usually requires: | back 43 D. Surface epithelial damage |
front 44 Low-risk HPV dysregulates growth via: | back 44 B. Notch pathway |
front 45 LSIL typically shows HPV replication that is: | back 45 C. High |
front 46 Most LSIL lesions: | back 46 A. Regress spontaneously |
front 47 In HSIL, HPV replication tends to be: | back 47 D. Low |
front 48 HSIL most characteristically shows: | back 48 C. Arrested epithelial maturation |
front 49 HSIL carries a: | back 49 B. High cancer progression risk |
front 50 A benign exophytic lesion causing spotting arises in the: | back 50 D. Endocervical canal |
front 51 Endocervical polyps contain: | back 51 C. Loose fibromyxoid stroma |
front 52 Endocervical polyps commonly present with: | back 52 B. Irregular bleeding/spotting |
front 53 Endocervical polyps are lined by: | back 53 A. Mucus-secreting endocervical glands |
front 54 HPV reaches target cells mainly through: | back 54 C. Epithelial breaks at SCJ |
front 55 HSIL reflects progressive cell-cycle deregulation by: | back 55 B. HPV |
front 56 Gartner duct cysts derive from: | back 56 D. Wolffian duct |
front 57 Which IHC pair is most associated with HPV-related SIL? | back 57 C. Ki-67 and p16 |
front 58 Why can Ki-67 appear in upper epithelium in HPV lesions? | back 58 A. E6/E7 block cell-cycle arrest |
front 59 Most common HPV type in both LSIL/HSIL? | back 59 D. HPV-16 |
front 60 About what fraction of LSIL is HPV-associated? | back 60 B. About 80% |
front 61 About what fraction of HSIL is HPV-associated? | back 61 A. Nearly 100% |
front 62 Most common histologic subtype of cervical cancer? | back 62 C. Squamous cell carcinoma |
front 63 Second most common cervical cancer type is: | back 63 B. Adenocarcinoma |
front 64 Precursor lesion for cervical adenocarcinoma? | back 64 D. Adenocarcinoma in situ |
front 65 Tumor with malignant glandular + squamous cells? | back 65 A. Adenosquamous carcinoma |
front 66 Which category tends to progress faster and worse? | back 66 C. Adenocarcinoma and neuroendocrine |
front 67 Advanced cervical carcinoma spreads mainly by: | back 67 B. Direct extension |
front 68 Cervical cancer confined to cervix is stage: | back 68 C. Stage I |
front 69 Carcinoma in situ (CIN III/HSIL) is stage: | back 69 A. Stage 0 |
front 70 Beyond cervix, not pelvic wall; vagina not lower third: | back 70 B. Stage II |
front 71 Pelvic wall involvement and lower third vagina: | back 71 D. Stage III |
front 72 Beyond true pelvis or bladder/rectum mucosa: | back 72 A. Stage IV |
front 73 Rectal exam shows no tumor-free space. Stage? | back 73 C. Stage III |
front 74 Hydronephrosis in cervical cancer suggests extension to: | back 74 B. Ureters |
front 75 HPV vaccination is routinely recommended for: | back 75 D. Girls and boys |
front 76 Anovulatory cycles cause endometrium exposure to: | back 76 C. Unopposed estrogens |
front 77 Anovulatory endometrium typically lacks: | back 77 A. Glandular secretory changes |
front 78 Another progesterone-dependent feature absent in anovulation: | back 78 D. Stromal predecidualization |
front 79 Progesterone is absent in anovulation because: | back 79 B. No corpus luteum forms |
front 80 Postpartum fever with uterine tenderness most suggests: | back 80 D. Acute endometritis |
front 81 Acute endometritis is most linked to infections after: A. Ovulation | back 81 B. Delivery or miscarriage |
front 82 Endometriosis is best defined as: | back 82 A. Ectopic endometrial tissue outside uterus |
front 83 Most common site for endometriosis is: | back 83 C. Ovaries |
front 84 A common endometriosis location is the: | back 84 B. Rectovaginal septum |
front 85 In HPV-related SIL, Ki-67 staining often extends into: | back 85 D. Upper epithelial layers |
front 86 Strong p16 staining most supports: | back 86 C. High-risk HPV infection |
front 87 Roughly what percent of cervical cancers are SCC? | back 87 A. About 80% |
front 88 Endometriotic stromal cells generate excess estrogen due to
increased: | back 88 C. Aromatase expression |
front 89 Endometriosis has been reported in men treated for prostate cancer
with: | back 89 A. High-dose estrogens |
front 90 A medication class beneficial in endometriosis targets which
enzyme? | back 90 D. Aromatase |
front 91 Which hormone most directly enhances persistence of endometriotic
tissue? | back 91 B. Estrogen |
front 92 A woman with endometriosis has higher risk for certain ovarian
cancers. The underlying condition is: | back 92 A. Endometriosis |
front 93 Likely precursor to endometriosis-related ovarian carcinoma: | back 93 C. Atypical endometriosis |
front 94 Adenomyosis is defined as endometrial tissue within the: | back 94 B. Myometrium |
front 95 Microscopy shows irregular stromal nests ± glands within uterine
wall. Diagnosis? | back 95 D. Adenomyosis |
front 96 Endometrial polyps can come from using: | back 96 C. Tamoxifen |
front 97 Tamoxifen’s tissue-selective action is best described as: | back 97 B. Antagonist breast, agonist endometrium |
front 98 A common cause of abnormal uterine bleeding and frequent precursor to
carcinoma: | back 98 D. Endometrial hyperplasia |
front 99 Endometrial hyperplasia is most strongly linked to: | back 99 A. Prolonged estrogenic stimulation |
front 100 The estrogen source driving hyperplasia may be: | back 100 B. Endogenous or exogenous |
front 101 Common genetic alteration in hyperplasia and endometrial
carcinoma: | back 101 D. PTEN inactivation |
front 102 PTEN loss most directly overactivates which pathway? | back 102 A. PI3K/AKT pathway |
front 103 Germline PTEN mutations causing high endometrial cancer risk: | back 103 C. Cowden syndrome |
front 104 Cowden syndrome is strongly associated with increased: | back 104 D. Breast and endometrial cancers |
front 105 Endometrial hyperplasia is classified as: | back 105 A. Non-atypical or atypical |
front 106 Atypical endometrial hyperplasia is also called: | back 106 C. Endometrial intraepithelial neoplasia |
front 107 Cardinal feature of non-atypical hyperplasia: | back 107 B. Increased gland-to-stroma ratio |
front 108 Atypical hyperplasia is best described as: | back 108 A. Complex glands with nuclear atypia |
front 109 Most common type of endometrial carcinoma: | back 109 D. Type I carcinoma |
front 110 Enzyme high in endometriotic stroma but absent in normal endometrial
stroma: | back 110 B. Aromatase |
front 111 Endometriosis increases risk of which ovarian cancer
subtypes? | back 111 C. Endometrioid and clear cell |
front 112 Estrogen’s main effect in endometriosis is to: | back 112 B. Enhance tissue survival |
front 113 A uterine wall lesion containing endometrial stroma ± glands is
located in the: | back 113 C. Myometrium |
front 114 Tamoxifen-associated endometrial polyps best reflect tamoxifen acting
as: | back 114 A. Weak endometrial estrogen agonist |
front 115 Complex gland crowding with nuclear atypia is: | back 115 A. Atypical hyperplasia |
front 116 Type I endometrial carcinomas are also called: | back 116 C. Endometrioid carcinomas |
front 117 Type I endometrioid carcinoma typically arises in the setting
of: | back 117 B. Endometrial hyperplasia |
front 118 Type I tumors share risk factors with hyperplasia, including: | back 118 A. Obesity and diabetes |
front 119 Atypical hyperplasia and endometrial carcinoma commonly share
mutations in: | back 119 B. PTEN |
front 120 This supports atypical hyperplasia as a: | back 120 B. Precursor to carcinoma |
front 121 Common mutations in type I endometrioid carcinomas increase signaling
through: | back 121 C. PI3K/AKT |
front 122 PI3K/AKT signaling in endometrial cells tends to augment: | back 122 B. Estrogen receptor targets |
front 123 Endometrioid carcinoma gross pattern can be: | back 123 D. Local polypoid or diffuse |
front 124 Typical spread for endometrioid carcinoma occurs via: | back 124 C. Myometrial invasion then extension |
front 125 Endometrioid adenocarcinomas are characterized by glands
resembling: | back 125 B. Normal endometrial epithelium |
front 126 Type II endometrial carcinomas most often arise in: | back 126 B. Endometrial atrophy |
front 127 Type II (serous) carcinomas are by definition: | back 127 B. Poorly differentiated |
front 128 Most common subtype of type II endometrial carcinoma: | back 128 C. Serous carcinoma |
front 129 Tumor suppressor mutated in ≥90% of serous carcinomas: | back 129 C. TP53 |
front 130 Precursor lesion of serous endometrial carcinoma: | back 130 B. Endometrial intraepithelial carcinoma |
front 131 Endometrial intraepithelial carcinoma consists of: | back 131 A. Cells identical to serous carcinoma |
front 132 Serous carcinomas often arise in: | back 132 B. Small atrophic uteri |
front 133 Serous carcinomas are often: | back 133 B. Bulky or deeply invasive |
front 134 Incidence of endometrial carcinoma peaks in: | back 134 D. Postmenopausal 55–65 |
front 135 Serous carcinoma occurs more frequently in women of: | back 135 B. African American descent |
front 136 Serous carcinoma contributes to mortality in African American women
being: | back 136 A. 2-fold higher |
front 137 Typical presenting symptom aiding early detection for Serous
carcinoma: | back 137 B. Postmenopausal vaginal bleeding |
front 138 For Serous carcinoma, Postmenopausal bleeding may occur with: | back 138 A. Excess leukorrhea |
front 139 Malignant mixed Müllerian tumors are typically: | back 139 B. Bulky/polypoid |
front 140 Histology of malignant mixed Müllerian tumor shows: | back 140 B. Adenocarcinoma + malignant mesenchyme |
front 141 Malignant mixed Müllerian tumors most often occur in: | back 141 B. Postmenopausal women |
front 142 Typical presentation of malignant mixed Müllerian tumors: | back 142 A. Vaginal bleeding |
front 143 Diagnosis of adenosarcoma requires: | back 143 B. Malignant stroma, benign abnormal glands |
front 144 Adenosarcomas are commonly seen in: | back 144 A. 4th–5th decade |
front 145 Adenosarcomas are generally: | back 145 B. Low grade malignancy |
front 146 Type I endometrioid tumors are associated with unopposed: | back 146 A. Estrogen stimulation |
front 147 Oophorectomy benefits endometrial stromal adenosarcoma because
of: | back 147 C. Estrogen withdrawal effect |
front 148 Low-grade endometrial stromal sarcoma commonly shows: | back 148 A. JAZF1–SUZ12 fusion |
front 149 JAZF1 most directly encodes a: | back 149 D. Transcriptional repressor |
front 150 SUZ12 is best linked to: | back 150 B. Repressive histone marks |
front 151 MED12 mutations occur in ~70% of uterine: | back 151 B. Leiomyomas |
front 152 MED12 mutations are virtually unique to: | back 152 D. Uterine smooth muscle tumors |
front 153 MED12 mutations are seen in: | back 153 A. Leiomyomas and leiomyosarcomas |
front 154 A uterine leiomyosarcoma most often metastasizes by: | back 154 C. Hematogenous spread |
front 155 Most typical distant metastasis site for leiomyosarcoma: | back 155 B. Lungs |
front 156 Distant spread pattern most consistent with leiomyosarcoma: | back 156 D. Lung, bone, brain |
front 157 Regurgitation theory of endometriosis proposes ectopic implants
via: | back 157 C. Retrograde menstrual flow |
front 158 “Benign metastases” theory proposes endometriosis spreads
via: | back 158 A. Blood and lymphatics |
front 159 Most common primary fallopian tube lesion: | back 159 D. Paratubal cysts |
front 160 Paratubal cysts are typically: | back 160 B. Translucent cysts, clear fluid |
front 161 Benign fallopian tube tumor is usually: | back 161 A. Adenomatoid tumor |
front 162 Tubal adenomatoid tumors often occur: | back 162 C. Subserosal or mesosalpinx |
front 163 Tubal adenomatoid tumor counterpart occurs in: | back 163 D. Testis or epididymis |
front 164 PCOS is best defined by: | back 164 A. Hyperandrogenism with chronic anovulation |
front 165 PCOS reflects dysregulation of enzymes in: | back 165 B. Androgen biosynthesis |
front 166 PCOS increases endometrial risk via increased free: | back 166 C. Estrone |
front 167 In PCOS, increased free estrone raises risk of: | back 167 D. Endometrial hyperplasia/carcinoma |
front 168 Stromal hyperthecosis is seen most often in: | back 168 B. Postmenopausal women |
front 169 Stromal hyperthecosis classically shows: | back 169 A. Bilateral uniform ovarian enlargement |
front 170 Microscopy in stromal hyperthecosis shows: | back 170 C. Hypercellular stroma, luteinization |
front 171 Virilization in stromal hyperthecosis is: | back 171 B. More striking than PCOS |
front 172 Cystic ovarian follicles can arise from: | back 172 D. Unruptured Graafian follicles |
front 173 Cystic follicles can also form when follicles: | back 173 A. Rupture then immediately seal |
front 174 Most primary ovarian neoplasms derive from: | back 174 B. Müllerian epithelium |
front 175 Benign ovarian tumor with cystic areas: | back 175 C. Cystadenoma |
front 176 Benign ovarian tumor with mainly fibrous areas: | back 176 A. Adenofibroma |
front 177 Benign ovarian tumor with cystic and fibrous areas: | back 177 D. Cystadenofibroma |
front 178 Stromal hyperthecosis is also called: | back 178 C. Cortical stromal hyperplasia |
front 179 An ovarian tumor described as borderline/malignant with a cystic
component is: | back 179 B. Cystadenocarcinoma |
front 180 Benign ovarian tumors are more common in: | back 180 A. Women age 20–45 |
front 181 Malignant ovarian tumors are more common in: | back 181 C. Women age 45–65 |
front 182 Type I ovarian carcinomas are typically: | back 182 A. Low-grade tumors |
front 183 Type I ovarian carcinomas often arise with: | back 183 A. Endometriosis or borderline tumors |
front 184 Type II ovarian carcinomas are best described as: | back 184 B. High-grade serous carcinomas |
front 185 Type II ovarian carcinomas arise from: | back 185 C. Serous intraepithelial carcinoma |
front 186 Most common malignant ovarian tumor type: | back 186 A. Serous tumors |
front 187 Serous tumors are typically: | back 187 B. Cystic neoplasms |
front 188 Germline mutations increasing ovarian cancer risk include: | back 188 D. BRCA1 and BRCA2 |
front 189 Low-grade serous carcinomas often arise with: | back 189 A. Serous borderline tumors |
front 190 High-grade serous carcinomas often arise from: | back 190 B. In situ lesions in fimbriae |
front 191 Serous tubal intraepithelial carcinoma (STIC) is associated with
sporadic: | back 191 B. High-grade serous ovarian cancers |
front 192 Women with BRCA mutation and strong family history may undergo: | back 192 B. Prophylactic salpingo-oophorectomy |
front 193 High-grade serous tumors commonly show mutations in: | back 193 C. TP53 |
front 194 Low-grade serous tumors more often show mutations in: | back 194 KRAS/BRAF/ERBB2 |
front 195 STIC lesions are identical to high-grade serous carcinoma except they
lack: | back 195 D. Invasion |
front 196 Mucinous tumors occur most frequently in: | back 196 B. Middle adult life |
front 197 Mucinous tumors rarely occur: | back 197 C. Before puberty or after menopause |
front 198 Mucinous tumors are: | back 198 C. Benign mostly |
front 199 A large unilateral ovarian mass shows mucinous epithelium. Which
mutation is most consistent? | back 199 A. TP53 mutation |
front 200 Which feature best fits mucinous ovarian tumors? | back 200 D. Surface rarely involved |
front 201 Histology shows tubular glands resembling endometrium. Tumor
type? | back 201 A. Endometrioid ovarian tumor |
front 202 Endometrioid ovarian carcinomas may coexist with: | back 202 C. Endometriosis |
front 203 Endometrioid carcinoma + endometriosis often share mutations
affecting: | back 203 B. PI3K/AKT and mismatch repair |
front 204 Endometrioid ovarian carcinomas are usually: | back 204 D. Low-grade tumors |
front 205 Large epithelial cells with clear cytoplasm suggest: | back 205 C. Clear cell carcinoma |
front 206 Transitional cell tumors of the ovary are usually: | back 206 A. Benign |
front 207 Ovarian carcinoma seeds peritoneum via capsule. Expected
finding? | back 207 D. Massive ascites |
front 208 Most ovarian carcinomas present with: | back 208 B. Lower abdominal pain, enlargement |
front 209 Benign ovarian teratomas are commonly called: | back 209 A. Dermoid cysts |
front 210 Mature (benign) teratoma is occasionally linked to: | back 210 C. Inflammatory limbic encephalitis |
front 211 A teratoma causes flushing and wheeze. Most likely syndrome? | back 211 B. Carcinoid syndrome |
front 212 An 18-year-old has malignant ovarian teratoma. Type? | back 212 A. Immature teratoma |
front 213 Most dysgerminomas are: | back 213 D. Unilateral tumors |
front 214 Rapidly growing pelvic mass in a child suggests: | back 214 C. Yolk sac tumor |
front 215 Ovarian choriocarcinoma (nongestational) is typically: | back 215 B. Chemo-resistant, often fatal |
front 216 Granulosa cell tumors are usually: | back 216 D. Unilateral, potentially malignant |
front 217 FOXL2 mutations are common in: | back 217 A. Adult granulosa tumors |
front 218 Tumors composed predominantly of theca cells are: | back 218 C. Almost always benign |
front 219 Plump spindle stromal cells with lipid droplets indicates: | back 219 B. Thecoma |
front 220 Most fibromas, fibrothecomas, and thecomas are: | back 220 A. Benign |
front 221 Over half of Sertoli-Leydig tumors show mutation in: | back 221 D. DICER1 |
front 222 DICER1 mutations primarily disrupt: | back 222 C. microRNA regulation |
front 223 A pregnancy-associated ovarian mass mimics corpus luteum.
Diagnosis? | back 223 A. Pregnancy luteoma |
front 224 Pregnancy luteoma may cause: | back 224 B. Virilization in female infants |
front 225 Metastatic GI carcinoma to ovaries is termed: | back 225 C. Krukenberg tumor |
front 226 Krukenberg tumor is classically: | back 226 D. Bilateral mucin signet-ring cells |
front 227 In mucinous ovarian tumors, laterality is most often: | back 227 A. Unilateral |
front 228 Clear cell ovarian carcinoma most resembles: | back 228 B. Hypersecretory gestation endometrium |